SUBARACHNOID HEMORRHAGE/BRAIN AUTOREGULATORY DYSFUNCTION

我们的具体目标是证明a)骚乱发生在 与血管痉挛无关的大脑微循环发展 蛛网膜下腔出血(SAH)后导致 脑血流量(CBF)和代谢减少；b) 这些骚乱表明在中国出现了混乱 脑血管自动调节，可能是延迟的原因之一 脑缺血；c)脑血流量和脑缺血的这些整体改变 新陈代谢是由去甲肾上腺素能的过度活动引起的 来自蓝斑(LC)的神经元投射 扩散到中枢神经系统的所有区域，并有 对局部脑代谢、脑血流、血管的深刻影响 通透性和大脑自动调节。 脑血流量、代谢活动、脑血管的变化 自动调节，大脑去甲肾上腺素将被定量 大鼠实验性蛛网膜下腔出血后。这些结果将是 比较有和没有事先破坏的动物的 LC.这些动物的脑血流量和新陈代谢将通过 14C-丁醇指示剂分级技术，以及 14C-脱氧葡萄糖放射自显影。脑组织中儿茶酚胺 将通过放射酶分析进行分析。 这些研究可能对描述 脑缺血后的病理生理作用 萨哈。这一结果可能会为患有糖尿病的患者提供新的治疗方法。 破裂的颅内动脉瘤。

Our specific aims are to demonstrate that a) disturbances in the cerebral microcirculation, unrelated to vasospasm, develop after subarachnoid hemorrhage (SAH) resulting in global reductions of cerebral blood flow (CBF) and metabolism; b) these disturbances are indicative of a disorder in cerebrovascular autoregulation, perhaps contributing to delayed cerebral ischemia; c) these global alterations of CBF and metabolism are induced by hyperactivity of the noradrenergic neurons derived from the locus coeruleus (LC), which projects diffusely to all regions of the central nervous system and have profound effects on regional cerebral metabolism, CBF, vascular permeability, and cerebral autoregulation. Changes in CBF, metabolic activity, cerebrovascular autoregulation, and brain norepinephrine will be quantitated following experimental SAH in rats. These results will be compared in animals with and without prior destruction of the LC. CBF and metabolism will be studied in these animals using a 14C-butanol indicator fractionation technique, and 14C-deoxyglucose autoradiography. Brain tissue catecholamines will be analyzed with a radioenzymatic assay. These studies might be significant in delineating pathophysiological contributions to cerebral ischemia after SAH. The results might suggest new approaches to patients with ruptured intracranial aneurysms.